Host-derived alleviates hyperuricemia by improving gut microbial community and hydrolase-mediated degradation of purine nucleosides.

The gut microbiota is implicated in the pathogenesis of hyperuricemia (HUA) and gout. However, it remains unclear whether probiotics residing in the host gut, such as , can prevent HUA development. Herein, we isolated SQ001 from the cecum of HUA geese and conducted in vitro assays on uric acid (UA) and nucleoside co-culture.

Lactobacillus rhamnosus GG ameliorates hyperuricemia in a novel model.

Hyperuricemia (HUA) is a metabolic syndrome caused by abnormal purine metabolism. Although recent studies have noted a relationship between the gut microbiota and gout, whether the microbiota could ameliorate HUA-associated systemic purine metabolism remains unclear. In this study, we constructed a novel model of HUA in geese and investigated the mechanism by which Lactobacillus rhamnosus GG (LGG) could have beneficial effects on HUA.

The active fraction from the tuber of inhibits melanoma B16 cells metastasis LPS-induced and .

This study was to identify anti-metastatic active fractions and compounds of (). The results indicated that 50 µg/mL ethyl acetate fraction () can dramatically inhibit mouse melanoma B16 cells migration and invasion . In B16 cells pulmonary and hepatic metastasis assays, 50 µg/mL alleviated mouse lung and liver weights, the number of metastatic nodules and the levels of TNF-α and IL-6 in mouse serum and organs.

Inhibition of p38 and ERK1/2 pathways by Sparstolonin B suppresses inflammation-induced melanoma metastasis.

Background: Cancer related inflammation plays a fatal role in the metastatic process, which can foster tumor growth, angiogenesis and dissemination. Sparstolonin B (SsnB), derived from Chinese medicine of the tubers of Scirpus yagara, is a TLR2 and TLR4 antagonists. It has exhibited multiple activities of anti-inflammatory, anti-cancer, anti-obesity and anti-hepatitis.

[A novel modi cation of real-time AS-qPCR by using locked nucleic acid-modified oligonucleotide probe as wild type allele amplification blockers for quantitative detection of the JAK2 V617F mutation].

Objective: To develop a novel real-time PCR for sensitively quantitative detection of JAK2 V617F allele burden in peripheral blood.

Methods: Based on the real-time allele-specific PCR (AS-qPCR), the locked nucleic acid (LNA)-modified oligonucleotide probe was used for selectively blocking amplification of wild-type alleles in AS-qPCR, and then a novel AS-LNA-qPCR method was established. The percentages of sample JAK2 V617F alleles were directly calculated by its threshold cycle (Ct) values according to the standard curve which generated by JAK2 V617F alleles with its Ct values.

[Detection of JAK2V617F mutation rate by real-time fluorescent quantitative PCR using allele specific primer and TaqMan-MGB probe for dual inhibiting amplification of wild type alleles].

This study was purposed to develop a real-time PCR assay for sensitive quantification of JAK2V617F allele burden in peripheral blood and to evaluate the clinical value of this method. Both allele-specific mutant reverse primer and wild-type TaqMan-MGB probe were used for dual-inhibiting amplification of wild-type alleles in a real-time PCR, and then the JAK2V617F mutant alleles were amplified specially. The standard curve for quantification of JAK2V617F was established by percentages of JAK2V617F alleles with threshold cycle (Ct) values in a real-time PCR.

[Cyclooxygenase inhibitors in some dietary vegetables inhibit platelet aggregation function induced by arachidonic acid].

The study was purposed to investigate whether the cyclooxygenase inhibitors from some dietary vegetables can inhibit platelet aggregation function by the arachidonic acid (AA). The vegetable juice was mixed with platelet rich plasma (PRP), and asprin was used as positive control. The maximum ratio of platelet aggregation induced by AA was measured on the aggregometer; heme and cyclooxygenase-1 (COX(1)) or cyclooxygenase-2 (COX(2)) were added to test tubes containing COX reaction buffer, the mixture was vortex-mixed and exposed to aspirin or vegetable juice, followed by addition of AA and then hydrochloric acid (1 mol/L) was added to stop the COX reaction, followed by chemical reduction with stannous chloride solution.